Several muscle disorders exist in which the etiology is unknown. Technology has now enabled researchers to investigate development of muscle tissue in vivo in mice. Mice that lack a functional myogenin gene have a greatly reduced number of muscle fibers at the time of birth. This transcription factor is believed to be involved in the process of differentiation of myoblasts to myotubes. At present, very little is known as to how myoblasts perceive the environment and if lateral signalling is needed in order for myoblasts to fuse. This proposal examines the question of cell autonomy by determining if wild-type myoblasts can rescue myogenin-null myoblasts through the use of chimeric mice. This will be accomplished through the following specific aims: 1. Myogenin-mutant embryonic stem (ES) cell lines carrying a ubiquitously expressing LacZ gene will be generated. 2. Chimeric embryos of varying degrees of chimerism will be derived from the assessed as to the contribution of the mutant phenotype to the muscle fibers employing the use of LacZ gene. If wild-type cells can rescue mutant cells, then the myogenin-null phenotype is not cell-autonomous and indicates that signalling between cells occur during muscle differentiation.